Replicated chromatin curtails 53BP1 recruitment in BRCA1-proficient and BRCA1-deficient cells

DNA double-strand breaks can be repaired by non-homologous end-joining or homologous recombination. Which pathway is used depends on the balance between tumor suppressors 53BP1 and BRCA1 availability of an undamaged template for homology-directed repair. How cells switch from a 53BP1-dominated to BRCA1-governed recombination response as they progress through cell cycle incompletely understood. Here we reveal, using high-throughput microscopy applying single normalization control increased genome size replicate their DNA, that recruitment damaged replicated chromatin inefficient in both BRCA1-proficient BRCA1-deficient cells. Our results substantiate dual model unreplicated BRCA1–BARD1–dominated chromatin, which replication-coupled dilution 53BP1’s binding mark H4K20me2 functionally cooperates with BRCA1–BARD1–mediated suppression binding. More generally, suggest appropriate data, example, content, provides additional layers information, critical quantifying interpreting cellular phenotypes.